ICRP Ref 00/902/09

International Commission on Radiological Protection
Statement on RadonApproved by the Commission in November 2009

(1) The Commission issued revised recommendations for a System of RadiologicalProtection in 2007 (ICRP, 2007) which formally replaced the Commission’s 1990
Recommendations (ICRP, 1991) and updated, consolidated, and developed the additional
guidance on the control of exposure from radiation sources. The Commission has previously
issued recommendations for protection against radon-222 at home and at work in
Publication 65 (ICRP, 1993).
(2) The Commission has now reviewed recently available scientific information on thehealth effects attributable to exposure to radon and its decay products. The Commission’s
full review accompanies this Statement. As a result of this review, for radiological protection
purposes the Commission now recommends a detriment-adjusted nominal risk coefficient fora population of all ages of 8x10-10 per Bq h m-3 for exposure to radon-222 gas in equilibriumwith its progeny (i.e. 5x10-4 WLM-1). The Commission’s findings are consistent with othercomprehensive estimates including that submitted to the United Nations General Assemblyby the United Nations Scientific Committee on the Effects of Atomic Radiation(UNSCEAR, 2009).
(3) Following from the 2007 Recommendations, the Commission will publish reviseddose coefficients for the inhalation and ingestion of radionuclides. The Commission now
proposes that the same approach be applied to intakes of radon and progeny as that applied toother radionuclides, using reference biokinetic and dosimetric models. Dose coefficients will
be given for different reference conditions of domestic and occupational exposure, taking into
account factors including inhaled aerosol characteristics and disequilibrium between radonand its progeny. Sufficient information will be given to allow specific calculations to be
performed in a range of situations. Dose coefficients for radon and progeny will replace the
Publication 65 dose conversion convention which is based on nominal values of radiation
detriment derived from epidemiological studies comparing risks from radon and externalradiation. The current dose conversion values may continue to be used until dose coefficientsare available. The Commission advises that the change is likely to result in an increase ineffective dose per unit exposure of around a factor of two.
(4) The Commission reaffirms that radon exposure in dwellings due to unmodified
concentrations of radium-226 in the earth’s crust, or from past practices not conducted within
the Commission’s system of protection, is an existing exposure situation. Furthermore, theCommission’s protection policy for these situations continues to be based on setting a level ofannual dose of around 10 mSv from radon where action would almost certainly be warranted
to reduce exposure. Taking account of the new findings, the Commission has therefore
revised the upper value for the reference level for radon gas in dwellings from the value inthe 2007 Recommendations of 600 Bq m-3 to 300 Bq m-3. National authorities should
consider setting lower reference levels according to local circumstances. All reasonable
efforts should be made, using the principle of optimisation of protection, to reduce radon
Page 1 of 2

ICRP Ref 00/902/09

exposures to below the national reference level. It is noted that the World HealthOrganisation now recommends a similar approach (WHO, 2009).
(5) Taking account of differences in the lengths of time spent in homes and workplaces ofabout a factor of three, a level of radon gas of around 1000 Bq m-3 defines the entry point for
applying occupational protection requirements for existing exposure situations. In
Publication 103, the Commission considered that the internationally established value of1000 Bq m-3 might be used globally in the interest of international harmonization ofoccupational safety standards. The Commission now recommends 1000 Bq m-3 as the entry
point for applying occupational radiological protection requirements in existing exposure
situations. The situation will then be managed as a planned exposure situation.
(6) The Commission reaffirms its policy that, for planned exposure situations, any
workers’ exposure to radon incurred as a result of their work, however small, shall beconsidered as occupational exposure (see paragraph 178 of ICRP, 2007).

References
ICRP, 1991. 1990 Recommendations of the International Commission on RadiologicalProtection. ICRP Publication 60. Ann. ICRP 21 (1-3).
ICRP, 1993. Protection against Radon-222 at Home and at Work. ICRP Publication 65. Ann.
ICRP 23 (2).
ICRP, 2007. The 2007 Recommendations of the International Commission on RadiologicalProtection. ICRP Publication 103. Ann. ICRP 37 (2–4).
UNSCEAR, 2009. United Nations Scientific Committee on the Effects of Atomic Radiation(UNSCEAR). UNSCEAR 2006 Report. Annex E. Sources-to-Effects Assessment forRadon in Homes and Workplaces. New York: United Nations, 2009.
WHO, 2009. World Health Organisation (WHO). WHO Handbook on Indoor Radon: A
Public Health Perspective. WHO Press, Geneva, 2009.

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July 27, 2010

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Annals of the ICRPICRP PUBLICATION XXX

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Lung cancer risk from radon and progeny

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Editor……………………..

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PUBLISHED FOR

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[Elsevier logo]

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CONTENTSPREFACE ................................................................................................................................. 4
EXECUTIVE SUMMARY ...................................................................................................... 6
1. INTRODUCTION ........................................................................................................... 12
2. EPIDEMIOLOGY OF LUNG CANCER RISK ASSOCIATED WITHRESIDENTIAL EXPOSURES TO RADON AND RADON PROGENY ................ 14
2.1.
Introduction ............................................................................................................ 14
2.2.
Studies published since 1990 ................................................................................. 14
2.3.
Pooled studies......................................................................................................... 17
3. EPIDEMIOLOGY OF CANCER RISK ASSOCIATED TO RADON AND
RADON PROGENY EXPOSURE IN UNDERGROUND MINES .......................... 20
3.1.
Review of results since Publication 65 .................................................................. 20
3.2.
Summary of estimates of Excess Relative Risk per WLM .................................... 21
3.3.
Lung cancer risks from radon and smoking ........................................................... 23
4. ASSESSMENT OF THE DETRIMENT FROM RADON AND RADON
PROGENY EXPOSURE ............................................................................................ 24
4.1.
Risks other than lung cancer .................................................................................. 24
4.2.
Calculation of lung cancer lifetime risk estimates for underground miners .......... 25
4.3.
Comparison of results from underground mine and domestic exposures .............. 27
5. CONCLUSIONS ............................................................................................................. 29
REFERENCES ....................................................................................................................... 31
APPENDIX A. ........................................................................................................................ 35
Results from epidemiological studies of underground miners ........................................... 35
References for Appendix A ................................................................................................ 37
APPENDIX B.
Dosimetry ............................................................................................... 38
B.1. Radon ..................................................................................................................... 38
B.2. Thoron .................................................................................................................... 41
References for Appendix B ................................................................................................ 43

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ABSTRACTThis report reviews recent epidemiological studies of lung cancer risk linked to
exposure to radon and its progeny. It concentrates on the results from pooled
case-control studies of residential exposures and cohorts of underground miners
exposed to low levels of radon and radon progeny. Consistent with the approach
used in ICRP Publication 65 (1993), recent miner data are used to recommend arevised detriment-adjusted nominal risk coefficient of 5 10-4 per WLM (14 10-5
per mJ h m-3), replacing the ICRP Publication 65 value of 2.8 10-4 per WLM (810-5 per mJ h m-3). Furthermore, pooled analyses of epidemiological studies oflung cancer risk from residential exposures demonstrate a statistically significant
increase per unit of exposure below average annual concentrations of about 200
Bq m-3. The risk estimates derived from these pooled analysis are consistent withthose from underground miners and are sufficiently robust to enable protectionof the public to be now based on residential concentration levels. However, foroccupational protection purposes, dose estimates are required to demonstratecompliance with limits and constraints. Dose estimates also allow comparisons
between various sources of public exposure. ICRP Publication 65 recommended
that doses from radon and its progeny should be calculated using a doseconversion convention based on miner epidemiological studies. ICRP now
proposes to treat radon and radon progeny in the same way as otherradionuclides and will publish dose coefficients calculated using dosimetricmodels for use within the ICRP system of protection.

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A Task Group was appointed by ICRP Committee 1, with representation ofseveral members from Committee 2 and one member from Committee 4 to review
risks from alpha emitting radionuclides. The Commission subsequently asked theTask Group to concentrate initially on radon. This report reviews epidemiologicalstudies of lung cancer risk associated with the inhalation of radon and radon progeny
in homes and in underground mines.
The members of the Task Group were:
M. Tirmarche (Chairperson)
M. Blettner
E. Blanchardon
E. Ellis

J.D. Harrison
D. Laurier
J.F. Lecomte
J.W. Marsh

F. Paquet
N. Shilnikova
M. Sokolnikov

The corresponding members of this Task Group were:
B. Grosche

J. Lubin

C.R. Muirhead

Consultants providing advice were:
F. Bocchichio

L. Tomášek

D. Chambers

Reviewers of report drafts were:
J. Boice

D. Chambers

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The membership of Committee 1 during 2005-9 was:J. Preston (Chairman)
A. Akleyev
M. Blettner
R. Chakraborty
J. Hendry
W.F. Morgan

C.R. Muirhead
R Ullrich
D.L. Preston
W. Rühm
R.E. Shore
F.A. Stewart

M. Tirmarche
P-K. Zhou

The membership of Committee 2 during 2007-9 was:
H-G. Menzel (Chairman)
M. Balonov
V. Berkovski
W.E. Bolch
A. Bouville
G. Dietze

K.F. Eckerman
J.D. Harrison
N. Ishigure
P. Jacob
J.L. Lipsztein
F. Paquet

A.S. Pradhan
Y-Z. Zhou

The membership of Committee 1 during 2009-13 was:J. Preston (Chairman)
T. Azizova
R. Chakraborty
S. Darby
J. Hendry
W.F. Morgan

C.R. Muirhead
N. Nakamura
W. Rühm
S. Salomaa
A.J. Sigurdson
F.A. Stewart

D. Stram
M. Tirmarche
R. Wakeford
P-K. Zhou

The membership of Committee 2 during 2009-13 was:
H-G. Menzel (Chairman)
M. Balonov
D.T. Bartlett
V. Berkovski
W.E. Bolch
R. CoxG. Dietze
K.F. Eckerman
A. EndoJ.D. Harrison
N. Ishigure
R. Leggett

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J.L. Lipsztein
J. Ma
F. Paquet
N. Petoussi-Henss
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EXECUTIVE SUMMARY

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(a) Epidemiological studies of occupational exposures of miners and of domestic
exposures of the public have provided strong and complementary evidence of therisks of lung cancer following inhalation of radon and radon progeny. In the large
cohorts of underground miners, annual occupational exposures were considered forthe whole working period of each individual. Consequently, these studies are able toanalyse dose-response relationships taking account of time-dependent modifying
factors such as age at exposure and time since exposure. Lung cancer risk associatedwith domestic exposures to radon has been studied in a large number of case-control
studies, requiring estimates of radon exposure in houses over a period of 30 years
preceding lung cancer diagnoses. A weakness of such studies is that measurements
made during the study period are assumed to apply throughout the whole period of
exposure. An important strength, however, is that the residential studies often
include detailed interviews so that adjustments can be made, in the statisticalanalysis, for tobacco smoking as well as exposure to other potential lungcarcinogens in the home or at work.
(b) In 1998, the BEIR VI report presented a comprehensive analysis of available
miner cohorts (NRC, 1998). Recent studies of lung cancer in miners include
relatively low concentrations of radon and radon progeny, long duration of followup and good quality of individual exposure data (UNSCEAR, 2009). A recent
pooled analysis of the French and Czech miner cohorts also provided risk estimatesassociated with low levels and good quality of individual exposure (Tomášek et al.,2008a). These results, consistent with previous analyses of combined miner studies,demonstrate statistically significant associations between cumulative radon exposureand lung cancer mortality at levels of exposure as low as 50 Working Level Months(WLM), i.e. 180 mJ h m-3. On the basis of calculations of lifetime excess absoluterisk (LEAR), using Publication 103 (ICRP, 2007) reference background rates andrisk models from pooled analyses (NRC, 1998; Tomasek et al., 2008a), a detrimentadjusted nominal risk coefficient of 5 10-4 per WLM (14 10-5 per mJ h m-3) is now
recommended for radiological protection purposes. This nominal risk coefficientreplaces the Publication 65 value of 2.8 10-4 per WLM (8.0 10-5 per mJ h m-3).
(c) Three comprehensive publications have provided joint analyses of data fromdomestic case-control studies for Europe (Darby et al., 2005), North America(Krewski et al., 2005; 2006) and China (Lubin et al., 2004). Each joint analysis
demonstrated an increased risk of lung cancer with increasing domestic radon
concentration, considering exposures over a period of 30 years preceding thediagnosis of cancer. The estimates of an increase of lung cancer per unit ofconcentration in the three joint analyses are very close to each other and statisticallycompatible: the values obtained were 1.08, 1.10 and 1.13 per 100 Bq m-3. A
combined estimate calculated for Europe, North American and China was 1.09 per
100 Bq m-3 (UNSCEAR 2009). All of these results were obtained after adjustment
for smoking habits. It is noted also that the slope of the linear exposure-response
relationships increased to 1.11 per 100 Bq m-3 when the analyses focused on thosecases and controls with more complete estimation of cumulated individual exposure(UNSCEAR 2009) .
(d) The joint analyses also made adjustments to take account of uncertainties
associated with variations in radon concentration. For example, in the European
pooled analysis (Darby et al., 2005), taking account of such uncertainties increased
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the estimate of relative risk from 1.08 to 1.16 per 100 Bq m-3. Limiting the European
analysis to those cases and controls with a relatively low annual exposure, there isevidence of an increased risk below 200 Bq m-3. It is concluded that the residential
studies provide a reasonable estimate of lung cancer risk and a basis for risk
management related to low protracted radon exposures in homes, considering
cumulated exposure during a period of at least 25 years.
(e) Although comparisons are complex, the cumulated excess absolute risk oflung cancer attributable to radon and radon progeny estimated for residential
exposures appears to be consistent with that obtained from miners at low levels of
exposure.
(f) In the European pooled analysis of domestic exposures, a statisticallysignificant trend in lung cancer risk was observed among smokers and also
separately among non-smokers (Darby et al., 2006). Therefore radon has been
demonstrated to be a lung carcinogen even in the absence of smoking. However, due
to the dominating effect of tobacco use on lifetime risk of lung cancer, the excess
absolute risk of lung cancer attributable to a given level of radon concentration ismuch higher among lifelong cigarette smokers than among non-smokers.
(g) The control of domestic exposures can be based directly on lung cancer risk
estimates per unit exposure derived from epidemiological data, that is, in terms ofradon concentrations in homes.
(h) However, for the purposes of control of occupational exposures using dose
limits and constraints, estimates of dose per unit exposure are required. In ICRP
Publications 65 and 66 (ICRP, 1993; 1994), the effective dose per unit exposure toradon and radon progeny was obtained using the so-called dose conversion
convention. This approach compared the detriment per unit exposure to radon andits progeny with the total detriment associated with unit effective dose, estimatedlargely on the basis of studies of Japanese survivors of the atomic bombings (ICRP,
1993). The values given were 5 mSv per WLM (1.4 mSv per mJ h m-3) for workers
and 4 mSv per WLM (1.1 mSv per mJ h m-3) for members of the public.
(i) Doses from radon and radon progeny can also be calculated using different
dosimetric models. A review of published data on the effective dose per unit
exposure to radon progeny obtained using dosimetric models is included as
Appendix B of this report. Values of effective dose range from about 6 to 20 mSv
per WLM (1.7 to 5.7 mSv per mJ h m- 3), with results using the ICRP (1994) Human
Respiratory Tract Model (HRTM) in the range from about 10 to 20 mSv per WLM(3 to 6 mSv per mJ h m-3) depending on the scenario of exposure.
(j) ICRP has concluded that doses from radon and radon progeny should be
calculated using ICRP biokinetic and dosimetric models, including the HRTM and
ICRP systemic models. That is, radon and its progeny should be treated in the same
way as other radionuclides within the system of protection. ICRP will provide dosecoefficients per unit exposure to radon and radon progeny for different reference
conditions of domestic and occupational exposure, with specified equilibrium
factors and aerosol characteristics. Until dose coefficients are published, thepreviously recommended Publication 65 values should continue to be used. It should
be recognised, however, that the dose coefficients to be published will be larger by
about a factor of two or more.

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Case-control study
Type of epidemiological study design in which a group of subjects with thedisease of interest (the cases with lung cancer) is compared to a group of
subjects that are free of this disease (the controls) but have similar
characteristics (sex, attained age…). This type of epidemiological design
was especially used in indoor radon studies. For each individual, past
exposures are estimated from measurements of radon concentration incurrent and previously occupied dwellings.

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Cohort study
Type of epidemiological study design in which a population exposed toradon and radon progeny is followed over time for the occurrence of diseases(including lung cancer). This type of epidemiological design was especiallyused in underground miner studies. The exposure in time is considered foreach individual on an annual basis.
Dose conversion convention

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This method defined in ICRP Publications 65 (ICRP, 1993) was used torelate exposure to radon progeny expressed in WLM or J h m-3, to effective
dose expressed in mSv on the basis of equal detriment.

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Equilibrium equivalent concentration (EEC)
The activity concentration of radon gas, in equilibrium with its short-lived
progeny which would have the same potential alpha energy concentration as
the existing non-equilibrium mixture.

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Equilibrium factor, F
The ratio of the equilibrium equivalent concentration to the radon gas
concentration. In other words it is the ratio of potential alpha energy
concentration (PAEC) for the actual mixture of radon decay product to thatwhich would apply at radioactive equilibrium.

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Existing exposure situations

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A situation that already exists when a decision on control has to be taken,
including natural background radiation and residues from past practices thatwere operated outside the Commission’s recommendations.

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Human Respiratory Tract Model (HRTM)
Model used in ICRP Publication 66 (1994) to evaluate the deposition andclearance of inhaled particles in the respiratory airways as well as theresulting dose to the lung tissues.

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Planned exposure situations

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Planned exposure situations are situations involving the deliberate
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rise both to exposures that are anticipated to occur (normal exposures) and toexposures that are not anticipated to occur

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Potential alpha energy concentration (PAEC)
The concentration of short-lived radon or thoron progeny in air in terms of
the alpha energy emitted during complete decay from radon-222 progeny tolead-210 or from radon-220 progeny to lead-208 of any mixture of shortlived radon-222 or radon-220 in a unit volume of air.

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Radon progeny
The decay products of radon-222, used in this report in the more limitedsense of the short-lived decay products from polonium-218 throughpolonium-214. Radon progeny are sometimes referred to as “radon decay
products”.

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Reference level
In existing controllable exposure situations, this represents the level of doseor risk, above which it is judged to be inappropriate to plan to allow
exposures to occur, and below which optimisation of protection should be
implemented. The chosen value for a reference level will depend upon
prevailing circumstances of the exposure under consideration.

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Risk

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Risk relates to the probability that an outcome (e.g. lung cancer) will occur.
Terms relating to risk are grouped together here:

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Excess absolute risk
An expression of excess risk based on the assumption that the excess risk
from radiation exposure adds to the underlying (baseline) risk by anincrement dependent in dose but independent of the underlying natural or
background risk.. In this report lifetime excess absolute risk (LEAR) of lungcancer is computed.

•

Excess relative risk (ERR)
Relative risk – 1.

•

Relative risk
The ratio of the incidence rate or the mortality rate from the disease ofinterest (lung cancer) in an exposed population to that in an unexposed
population.

•

Risk coefficient
Increase of risk per unit exposure or per unit dose. In general, expressed as
ERR per WLM, per J h m-3, per 100 Bq m-3 or per Sv.

•

Risk model

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A model describing the variation of the risk coefficient as a function ofmodifying factors, such as time since exposure, attained age or age at
exposure. It may be related by a factor to the age specific baseline risk
(multiplicative) or added to the baseline risk (additive).

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Lifetime risk
Risk cumulated by an individual up to a given age. The estimate used in thepresent report is the Lifetime Excess Absolute Risk (LEAR) associated to achronic exposure scenario, expressed in number of death 10-4 per WLM (alsosometimes denominated as the Radiation Excess Induced Death REID). In
the present report, except if otherwise stated, the lifetime duration is 90 years
as generally considered in ICRP publications, and the scenario is a constant
low level exposure to 2 WLM per year during adulthood from 18 years to 64
years, as proposed in ICRP Publication 65 (ICRP, 1993).

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Detriment
Detriment is an ICRP concept. It reflects the total harm to health experienced
by an exposed group and its descendants as a result of the group’s exposure
to a radiation source. Detriment is a multi-dimensional concept. Its principal
components are the stochastic quantities: probability of attributable fatal
cancer, weighted probability of attributable non-fatal cancer, weighted
probability of severe heritable effects, and length of life lost if the harm
occurs.

•Detriment-adjusted risk
The probability of the occurrence of a stochastic effect, modified to allow for
the different components of the detriment in order to express the severity of
the consequence(s).

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Thoron progeny
The decay products of radon-220, used herein in the more limited sense of
the short-lived decay products from polonium-216 through polonium-212 orthallium-208.
Unattached fraction
The fraction of the potential alpha energy concentration of short-lived radon
progeny that is not attached to the ambient aerosol.

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Upper reference levels

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Maximum values of exposure under which ICRP recommends national
authorities to establish their own national reference levels.

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Working level (WL)
Any combination of the short-lived progeny of radon in one litre of air thatwill result in the emission of 1.3 x 105 MeV of potential alpha energy. 1 WL
= 2.08 10-5 J m-3.

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Working Level Month (WLM)
The cumulative exposure from breathing an atmosphere at a concentration of
1 working level for a working month of 170 hours.

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Joules (J) :354

Potential alpha energy concentration:

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Radon progeny :1 Bq m-3 of radon at equilibrium = 3.47 104 MeV m-3 = 5.56 10-9 J m-3
Thoron progeny :1 Bq m-3 of thoron at equilibrium = 4.72 105 MeV m-3 = 7.56 10-8 J m-3
Working level:360

1 WL = 1.3 108 MeV m-3

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Working level month (WLM) :363

1 WLM = 3.54 10-3 J h m-3364

1 WLM = 6.37 105 Bq h m-3 EEC of radon

365

1 WLM = 6.37 105/F Bq h m-3 of radon(a)366

1 Bq m-3 of radon during 1 year = 4.4 10-3 WLM at home(b)367

1 Bq m-3 of radon during 1 year = 1.26 10-3 WLM at work(b)368

1 WLM = 4.68 104 Bq h m-3 EEC of thoron

369(a) F = equilibrium factor

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(b) Assuming 7000 h per year indoors or 2000 hours per year at work and an
equilibrium factor of 0.4 (ICRP, 1993).

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1. INTRODUCTION

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(1) Radon-222 is a naturally occurring radioactive gas, with a half-life of 3.8
days. It is formed as the decay product of radium-226 (half-life 1600 years), which
is a member of the uranium-238 decay chain. Uranium and radium occur naturally insoil and rocks and provide a continuous source of radon. Radon gas emanates fromthe earth’s crust and as a consequence is present in the air outdoors and in allbuildings, including workplaces. There is a large variation of indoor air
concentrations of this gas, depending mainly on the geology of the area and factorsthat affect the pressure differential between the inside and outside of the building,such as ventilation rates, heating within the building and meteorological conditions.
(2) Because radon is inert, nearly all of the gas that is inhaled is subsequently
exhaled. However, 222Rn decays into a series of solid short-lived radioisotopes
which deposit within the respiratory tract. Because of their relatively short half-lives(less than half an hour), the radon progeny decay mainly in the lung before clearance
can take place. Two of these short-lived progeny, polonium-218 and polonium-214,
emit alpha particles and it is the energy from these alpha particles that dominates
dose to the lung and the associated risk of lung cancer.
(3) The historical unit of exposure to radon progeny applied to the uranium
mining environment is the working level month (WLM) which is related to thepotential alpha energy concentration of its short-lived progeny. One WLM is definedas the cumulative exposure from breathing an atmosphere at a concentration of 1
working level (WL) for a working month of 170 hours. A concentration of 1 WL is
any combination of the short-lived radon progeny in one litre of air that will result in
the emission of 1.3 105 MeV of alpha energy. One WLM is equivalent to 3.54 10-3 J
h m-3 in SI units. Exposures can also be quantified in terms of the activity
concentration of the radon gas in Bq h m-3. The two units are related via theequilibrium factor, F, which is a measure of the degree of disequilibrium between
radon and its short-lived progeny (1 WLM = 6.37 105 / F Bq h m-3; 1 J h m-3 = 1.8
108 / F Bq h m-3). Thus, an annual domestic exposure of 227 Bq m-3 gives rise to
1 WLM, assuming occupancy of 7000 h y-1 and F value of 0.4.
(4) Radon has long been recognised as a cause of lung cancer and it was
identified as a human lung carcinogen in 1986 by the World Health Organisation(WHO, 1986; IARC, 1988). The main source of information on risks of radoninduced lung cancer has been epidemiological studies of underground miners (ICRP,
1993), and more recent studies have provided informative data on risks at lower
levels of exposure (e.g., Lubin et al., 1997b; NRC, 1998; EPA, 1999; 2003,
Tomášek et al., 2008a). In addition, recent combined analyses of data from casecontrol studies of lung cancer and residential radon exposures have demonstrated
raised risks (Darby et al., 2005; 2006; Krewski et al., 2006; Lubin et al., 2004).
(5) A complication in the specification and control of doses and risks fromradon has been that doses can be calculated in two ways: the so-called“epidemiological” approach and the “dosimetric” approach. Publication 65 (ICRP,
1993) recommended an epidemiological approach in which the risk of fatal lungcancer per unit radon exposure (in J h m-3 or WLM) was compared with the totalrisk, expressed as detriment, per unit effective dose (in Sv). Hence, values of mSv(effective dose) per mJ h m-3 or WLM were obtained and referred to as the doseconversion convention. Alternatively, various dosimetric models of the humanrespiratory tract, including the ICRP (1994) model can be used to estimate
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equivalent dose to the lungs and effective dose per unit radon and radon progeny
exposure. Given the uncertainties inherent in the estimation of risks from radiation
exposure, and in the calculation of doses using dosimetric models, it is not
surprising that the two approaches to calculating effective dose per unit radon
exposure have resulted in different values. In fact, the differences are remarkably
small. However, the use of different values by different organisations, notably by
ICRP (1993) and UNSCEAR (2000) suggests the need for clarification and theformulation of a consistent approach. ICRP now intends to treat radon and its
progeny in the same way as other radionuclides and publish dose coefficients
calculated using models for use within the ICRP system of protection.
(6) This report considers epidemiological data on radon risks published since
ICRP Publication 65 (ICRP, 1993) focusing on studies involving low levels of
protracted exposure. Results of pooled residential case-control studies are discussed
in Chapter 2 and results of recent miner epidemiological studies with low exposures
are discussed in Chapter 3. The miner data are used to recommend a revised estimateof lung cancer lifetime risk per unit radon progeny exposure at low protracted levelsof exposure to radon and its progeny. Appendixes provide additional information on
epidemiological results obtained from miner studies (Appendix A) and review
published results of dose per unit exposure to radon progeny and thoron progeny,
calculated using dosimetric models of the human respiratory tract (Appendix B).

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2. EPIDEMIOLOGY OF LUNG CANCER RISK ASSOCIATED WITHRESIDENTIAL EXPOSURES TO RADON AND RADON PROGENY

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2.1. Introduction

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(7) In 1988, the International Agency for Research on Cancer (IARC, WHO)
classified radon as a human lung carcinogen, based on a review of evidence fromexperimental data on animals and from epidemiological studies of undergroundminers exposed to relatively high radon and radon progeny concentrations. This
report is focussed on those epidemiological studies able to provide information on
the dose-response relationship between lung cancer risk at relatively low annual
exposures to radon and radon progeny. Studies which include both individual
exposure assessment and individual assessment of potential confounding factors or
co-factors, such as tobacco use, are given special emphasis. Ecological studies ofcancer rates and average exposure per country or per region do not provide
individual exposure data and are not considered: they are unable to provide reliable
information on risk and are limited due to the unknown effect of confounding
factors, including smoking, and the unknown influence of population movement intoand out of the study areas (WHO, 1996; NRC 1998).
(8) The applicability of studies of underground miners to estimate
radon-induced lung cancer for residential concentrations of radon has been an
important uncertainty over the last twenty years. A variety of factors need to beconsidered in this extrapolation from mines to homes, including the linearity of thedose-response relationship, any differences between risks for adult males and thegeneral population which includes women and children, the difference in otherenvironmental exposures which may include arsenic, quartz and diesel exhaust
amongst others, different equilibrium factors between radon and its short-lived
progeny, and different breathing rates.
(9) Because of the desirability of having direct information on risks associatedwith domestic radon concentrations, a large number of residential epidemiologicalstudies were launched in the late 1980s and early 1990s. There was also anawareness that pooling of data may be required to provide the statistical power todemonstrate a significant risk at residential exposure concentrations (Lubin et al.,1997a). Reliable estimates of individual exposure conditions over long periods oftime were an important prerequisite of the epidemiological studies, with long-termradon measurement in the current and previous homes of each individual.
Individuals’ habits and ventilation conditions in dwellings had to be considered.

478

2.2. Studies published since 1990

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481
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485
486
487

(10) This section includes analytical epidemiological studies that have been
published since 1990 that have included at least 200 lung cancer cases, as well as
long-term domestic radon measurements. Selected studies are listed in Table 2.1;
more extensive details are available elsewhere (UNSCEAR, 2009).
(11) In most of the studies, year-long measurements of radon and its decay
products were made using standard methodologies in order to integrate any
variations in the specific conditions of the dwellings and any climatic and seasonalchanges. Most measurements are of concentrations in air using alpha track detectors.
In a few studies, glass-based retrospective detectors were also used.
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(12) A number of European studies were designed with the intention of
conducting a pooled analysis (see Section 2.3). Considerable efforts were made tohave comparable protocols before starting studies in different countries. They were
all case-control studies, with face-to-face interviews whenever possible of both thecases (lung cancer patients) and the controls (hospital controls or controls from thegeneral population). The same detailed questionnaire was used to analyse lungcancer risk in relation to domestic radon exposure, adjusting for tobacco
consumption, occupational exposures, and indicators of socio-economic status.
These studies provide information on lung cancer risks from radon, for smokers andnon-smokers, and allow adjustment to be made relating to years as a smoker, the age
smoking began, years since stopping smoking, and the number of cigarettes per day.
Several large case-control studies were also conducted in Canada and in the USA, as
well as two studies in China, one in Shenyang and one in Gansu. Table 2.1
summarizes 20 studies published between 1990-2006.

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Table 2.1. Residential radon cases-controls studies and one cohort study with morethan 200 lung cancer cases published between 1990 and 2006

Reference

RegionPopulation

No of Cases / Controls

Measurement. Relative risk perperiod100 Bq/m3

Schoenberg et al.,
1990

USA (New Jersey)

Women

480 cases, 442 controls

1 year

1.49

0.89-1.89

Blot et al., 1990

China-Shenyang

Women

308 cases, 356 controls

1 year

0.95

undefined-1.08

Pershagen et al., 1992

SwedenWomen

201 cases, 378 controls

1 year

1.16

0.89-1.92

Pershagen et al., 1994

Sweden-1281 cases, 2576 controls

3 months

1.10

1.01-1.22

Letourneau et al.,
1994

Canada-738 cases, 738 controls

1 year

0.98

0.87-1.27

Alavanja et al., 1994

USA (Missouri)

Women,
never-smokers

538 cases, 1183 controls

1 year

1.08

0.95-1.24

Auvinen et al., 1996

Finland-

517 cases, 517 controls

1 year

1.11

0.94-1.31

Ruosteenoja et al.,
1996

South FinlandMen

318 cases, 1500 controls

2 months

1.80

0.90-3.50

Darby et al., 1998

United Kingdom-

982 cases, 3185 controls

6 months

1.08

0.97-1.20

Alavanja et al., 1999

USA (Missouri)

Women

477 cases, 516 controls

1 year

1.27

0.88-1.53

1.3

1.07-2.93

387 cases, 473 controls

95 % CI

Field et al., 2000

USA (Iowa)

Women

413 cases, 614 controls

1 year

1.24

0.95-1.92

Kreienbrock et al.,2001

Germany (West)-1449 cases, 2297 controls

1 year0.97

0.82-1.14

Lagarde et al., 2001

SwedenNeversmokers

436 cases, 1649 controls

3 months

1.10

0.96-1.38

Wang et al., 2002

China-Gansu-

768 cases, 1659 controls

1 year

1.19

1.05-1.47

Kreuzer et al., 2003

Germany (East)-

1192 case, 1640 controls

1 year

1.08

0.97-1.20

Baysson et al., 2004

France-486 cases, 984 controls

6 months

1.04

0.99-1.11

Bochicchio et al.,
2005

Italy

-

384 cases, 404 controls

6 + 6 months

1.14

0.89-1.46

Sandler et al., 2006

USA(Connecticut +(Utah-South Idaho)-

1474 cases,1811 controls

1 year

1,01

0.79-1.21

Tomášek et al., 2001

Czech republic-

173 cases in a cohort of
000 inhabitants

1 year

1.10

1.04-.1.17

506
507
508
509
510
511
512
513
514
515
516
517

CI: confidence interval;- = men and women

12(13) The studies listed in Table 2.1 evaluated the association between lungcancer and domestic radon exposure. Results are presented in terms of the relativerisk per 100 Bq m-3 averaged for most studies over 20 to 30 years prior to lungcancer diagnosis Two studies considered only never-smokers; most studies
considered males and females, smokers and non-smokers. Risks of radon exposure
are adjusted for smoking habits, and in several studies are also adjusted for
occupational exposures known to be potential lung carcinogens (e.g. exposure toasbestos). Most of the twenty studies (17 out of 20 independent studies) reported apositive trend in lung cancer risk with increasing exposure, but few of the trends
were statistically significant. A few studies were also consistent with the absence ofa positive trend. Each study considered alone had low statistical power and provided
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an estimate of the risk per unit of exposure with a large confidence interval. Most of
the studies included only a small number of lung cancer cases that were neversmokers and thus were limited in evaluating associations between radon decay
products and lung cancer in non-smoking populations.
(14) In most studies, there were some residences in which radon concentration
could not be measured, e.g. if the house had been demolished. Radon concentrations
for such missing periods needed to be estimated for the purposes of the statisticalanalyses. Even when radon had been measured in a home, the measurements were
subject to uncertainty in the sense that repeated measurements in the same residence
and in the same period showed a high variability of radon levels. The inability todetect an association in many individual studies may have been due to poor
retrospective radon exposure assessment and/or to there being only very few casesand controls living in residences with high radon concentrations over 200 Bq m-3. In
several studies the average time weighted radon concentrations in homes occupied
by cases and controls were low, and only a few studies (e.g. in the Czech republic,
Finland, France, Sweden and Gansu, China) included persons living in relatively
high levels of exposure, above 400 Bq m-3.
2.3.

Pooled studies(15) Since 2000, several joint analyses were published, integrating the basic datafrom individual case and control subjects and applying a standard methodology,
both in defining selection criteria and statistical analysis. It is noted that several
informative meta-analyses of radon studies have been conducted but did not havethe strengths of these pooled analyses which handle individual data in the samemanner (Lubin 1997a; NRC 1998; UNSCEAR 2009). Three joint analyses havebeen conducted based on data from Europe (Darby et al., 2005), North America(Krewski et al., 2005; 2006) and China (Lubin et al., 2004) (Table 2.2). Each joint
analysis showed evidence of lung cancer risk, increasing with cumulated domestic
exposure to radon. The exposure period considered was at least 30 years prior to
diagnosis for the North American and Chinese joint analysis and 35 years for theEuropean joint analysis. In each analysis the radon concentrations estimated for the
5 years prior to diagnosis were not considered since a minimum lag time of 5 years
was assumed from lung cancer induction to diagnosis based on data from studies ofunderground miners (NRC 1998). In consequence the estimated risk per unit of
exposure is based on a time weighted average exposure for a window period 5 to 30
years prior to diagnosis (5 to 34 years for the European pooled analysis). The
estimates of the increase of lung cancer per unit exposure in the three joint analyses
are very close to each other and statistically compatible (Table 2.2): the values
obtained were 1.08, 1.10 and 1.13 per 100 Bq m-3 for Europe, America and China,
respectively. The combined estimate for Europe, North American and China was
1.09 per 100 Bq m-3 (UNSCEAR 2009).
(16) The relative risk of lung cancer was shown to be increased among both
smokers and non-smokers. In the European joint analysis, the estimated relative risk
per 100 Bq m-3 was 1.11 (95%CI : 1.00-1.28) for life long non–smokers; in the joint
North American study, the relative risk for non-smokers was of the same level; 1.10,
but not statistically significant (95%CI : 0.91-1.42).
(17) It is noteworthy that the slope of the linear exposure-response relationships
increased when analyses were restricted to those cases and controls with more
precise estimates of cumulated individual exposure, for example, if data were17

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considered only for individuals resident in the same house for the previous twenty
years. In the North American study (Krewski et al., 2005; 2006), analysis restricted
on residential stability (i.e. only 1 – 2 houses occupied in the 5 - 30 years preceding
diagnosis) and completeness of radon monitoring (measurements for at least
20 years of the considered period), resulted in an increase in relative risk from 1.10
to 1.18 per 100 Bq m-3. In the Chinese analysis (Lubin et al., 2004), when
considering only those subjects living in their current homes for 30 years or more,
the relative risk increased from 1.13 to 1.32 (1.07-1.91). According to the
UNSCEAR 2006 report, for all three joint analyses combined the slope of the linear
exposure-response relationships increased to 1.11 per 100 Bq m-3 when the analyses
focused on those cases and controls with more precise estimates of cumulated
individual exposure (UNSCEAR 2009).
(18) The joint analyses tried also to take account of uncertainties associated withvariations in exposure (Fearn et al., 2008). In the European pooled analysis (Darbyet al., 2005; 2006), taking account of random uncertainties in radon measurements
increased the estimate of the relative risk from 1.08 to 1.16 per 100 Bq m-3.
(19) Limiting the European analysis to those cases and controls with a relatively
low annual exposure, there is convincing evidence of an increased risk for those
exposed to levels below 200 Bq m-3 (Darby et al., 2006).
(20) One of the strengths of these joint analyses is that efforts were made tocollect detailed past smoking habits on the basis of direct interviews in most studies
and each analysis included adjustment for smoking. For the European pooling(Darby et al., 2005; 2006), a negative correlation between residential radon andsmoking was demonstrated, meaning that failure to take account of smoking would
have biased the estimates of risks from radon towards the null. The relative risk oflung cancer per 100 Bq m-3 was 1.02 when stratifying by study, region, age and sex,
but not smoking. This estimate increased to 1.05 after additionally stratifying forsmoking using seven categories (never-smokers; current cigarette smokers of <15,
15-24 or >25 cigarettes per day; ex-smokers of <10years or >10 years duration; andunknown). A further increase to 1.08 was observed when current smokers were
further stratified by age at starting smoking and ex-smokers were stratified by the
number of cigarettes smoked.

Table 2.2 Pooled analyses of case-control studies of residential exposure to radonand lung cancer, based on measured radon concentrations
Joint analysis
European(Darby et al., 2006)
North American

Number of
Number of Number ofstudies included
cases
controls
13
7148
14208
7

3662
18

4966

Relative risk per 100
Bq m-3 (95% CI)
1.08 (1.03-1.16)
1.10 (0,99-1.26)

DRAFT REPORT FOR CONSULTATION(Krewski et al., 2006)

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650
651

Chinese(Lubin et al., 2004)

2

1050

1995

1.13 (1.01-1.36)

CI: confidence interval(21) In conclusion, the joint analyses of lung cancer risk from residential radon
exposures show an increase in risk of at least 8 % per 100 Bq m-3, considering aperiod of exposure from 5 up to 30 - 35 years preceding the date of cancer diagnosis.
Confining analysis to those with presumably more precise exposure measurements,
the observed risk is increased in each of the joint analyses. The European poolingreported an excess relative risk increase of 16% per 100 Bq m-3 when uncertainties
in the measured radon activity concentrations were considered. This value may beconsidered as a reasonable estimate of the risk associated with relatively low andprolonged radon exposures in homes, considering an exposure over a period of 25 30 years.
(22) When the analysis is limited to lifelong non smokers, a statisticallysignificant positive trend is still observed in the European pooling, based on a large
number of lung cancer cases: 268 in men and 616 cases in women and on more than
5000 controls (Darby et al., 2006).
(23) On the basis of the results of the European pooling, the cumulative risk oflung cancer up to 75 year of age is estimated for lifelong non-smokers as 0.4%,
0.5% and 0.7% for radon activity concentrations of 0, 100 and 400 Bq m-3,
respectively. Lifelong cigarette smokers have a much higher baseline risk of lungcancer that is about 25 times higher than for non-smokers. The lifetime cumulative
risks of lung cancer by age 75 for lifelong smokers are close to 10%, 12% and 16%
for radon activity concentrations of 0, 100 and 400 Bq m-3, respectively, and reflect
the dominating effect of tobacco use on lifetime risk of lung cancer with or withoutradon contribution.
(24) A “world pooling” analysis is in progress under the coordination of Sarah
Darby (Oxford University), considering more then 13,700 lung cancer cases from 25
studies; it will include three supplementary studies: one from Russia (Urals) and two
from North America (Massachusetts and New Jersey). Results from this large joint
analysis are expected in the near future. They may provide better adjustments forcofactors, but as the dominant studies included are considered here in the three
separate joint analyses from Europe, North America and China, the overall
conclusion is expected to be the same: clear evidence of an increased relative risk oflung cancer related to radon exposure cumulated in houses during a residence periodof at least 30 years prior to the diagnosis.

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3. EPIDEMIOLOGY OF CANCER RISK ASSOCIATED TO RADON AND
RADON PROGENY EXPOSURE IN UNDERGROUND MINES

654

3.1. Review of results since Publication 65

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(25) ICRP Publication 65 (ICRP, 1993) estimated the risk of lung cancer deathfrom radon exposure on the basis of studies on seven cohorts of miners (Colorado
USA, Ontario Canada, New Mexico USA, Beaverlodge Canada, Western Bohemia
Czech Republic, CEA-COGEMA France and Malmberget Sweden) (Table A1 in
Appendix A). The total number of miners was 31,486. The weighted average of theexcess relative risk (ERR) per 100 WLM for these studies was 1.34 (95%CI = 0.822.13). This ERR coefficient applied to a follow-up period of 20 years, taking into
account a lag-time (minimum latency) of 5 years, i.e., radon results for exposuresexperienced 5 years prior to death from lung cancer (or comparable date for otherminers) are excluded from the analyses. A model was derived, taking account of themodifying effects of age at exposure and time since exposure (ICRP, 1993).
(26) A comprehensive analysis of epidemiological results based on 11 cohorts ofradon-exposed miners was published in 1994 (Lubin et al., 1994). In comparison to
the ICRP Publication 65 report, results for some cohorts were updated (Colorado
USA, Ontario Canada, Beaverlodge Canada, Western Bohemia, Czech Republic andMalmberget Sweden) and other cohorts were added (Yunnan China, Newfoundland
Canada, Port Radium Canada, and Radium Hill Australia). This analysis gave an
ERR per 100 WLM of 0.49 (95% CI = 0.2-1.0) (Lubin et al., 1994). After someminor updates of the same 11 cohorts, a new joint analysis was published in the
BEIR VI report (NRC, 1998). This joint analysis relied on a total of 60,606 miners,
with a total of 2,674 lung cancer deaths (Table A2 in Appendix A). The estimatedcombined ERR per 100 WLM was 0.59, assuming an exposure lag-time of 5 years.
Two models were derived, taking account of modifying effects of age at exposureand time since exposure, as well as either duration of exposure or mean rate of
exposure. Analyses on restricted ranges of cumulative exposure of less than 100 or
50 WLM were also performed (NRC, 1998).
(27) Since the BEIR VI report (NRC, 1998), new results have been published
for the West-Bohemian cohort (uranium mines) and North Bohemian cohort (tinmines) in the Czech Republic (Tomášek and Placek, 1999; Tomášek, 2002;
Tomášek et al., 2003; Tomášek and Zarska, 2004), the Newfoundland cohort(fluorspar mines) (Villeneuve et al., 2007) and the Eldorado cohort (including
workers from Port Radium and Beaverlodge) (Howe, 2006) in Canada, the Colorado
Plateau cohort (Schubauer-Berigan et al., 2009) in the US, the Wismut uranium
mines in Germany (Kreuzer et al., 2002; Grosche et al., 2006; Kreuzer et al, 2008)
and the CEA-COGEMA mines in France (Rogel et al., 2002; Laurier et al., 2004;
Vacquier et al., 2008; Vacquier et al., 2009).
(28) The UNSCEAR 2006 (2009) report provided a comprehensive review ofavailable epidemiological results from nine studies (the New Mexico USA andAustralian studies were not included), including a total of more than 126 000 miners(Table A3 in Appendix A). The weighted mean average ERR per 100 WLM was
0.59 (95%CI = 0.35-1.0) (UNSCEAR, 2009).
(29) Since the UNSCEAR 2006 (2009) report, the results of a joint analysis of
the Czech and French miner cohorts have been published. This analysis included
10,100 miners with a relatively long follow-up (mean, about 24 years) and relatively
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low levels of cumulative exposure (mean, 46.8 WLM). The estimated ERR per 100
WLM was 1.6 (95%CI = 1.0-2.3) (Tirmarche et al., 2003; Tomášek et al., 2008a).
(30) Although other miner studies have been published, they are generally notincluded here or in other comprehensive summaries since they provide little to noquantitative information on the relationship between radon and cancer risk.

704

3.2. Summary of estimates of Excess Relative Risk per WLM

705
706
707
708
709
710
711
712
713
714
715
716
717
718
719

The results from combined analyses summarised in Table 3.1 are presented as
simple linear estimates of the ERR per WLM. They apply across the whole
population of the cohorts under consideration but do not reflect variations of risk
between or within the cohorts. Some characteristics of the cohorts may explain
variations in the estimated ERR per WLM, including duration of follow-up, attained
age, duration of work, exposure levels and background rates of lung cancer. It is
important, therefore, to consider such factors in the assessment of the risk associatedwith radon and radon progeny exposure. Nevertheless, the three large-scale analyses
that summarise most currently available information (Lubin et al., 1994; NRC, 1998;
UNSCEAR, 2009) provide estimates of the association between cumulated WLM
exposure and lung cancer risk that are highly concordant.
Table 3.1 Summary of Excess Relative Risk per WLM published from combined
analyses of miners studies
No. ofcohorts7

No. ofminers
31 486

Personyears
635 022

ERR per
100 WLM
1.34

Lubin et al., 1994

11

60 570908 903

0.49

NRC, 1998

11

60 705892 547

0.59

UNSCEAR, 20099

125 627

3 115 975

0.59

0.35 – 1.00

Tomášek et al., 2008a2

10 100248 782

1.60

1.00 – 2.30

Reference
ICRP, 1993

720
721
722
723
724
725
726
727
728
729
730
731
732
733
734
735
736
737

SE: standard error

SE

95% CI
0.82 – 2.13
0.20 - 1.00

1.32

CI: confidence interval(31) All of the combined analyses and some of the individual studies
demonstrate a modifying effect of time since exposure (TSE) and, to a lesser extent,of age at exposure (AE) (ICRP, 1993; Lubin et al., 1994; NRC, 1998; Howe, 2006;
Tomášek et al., 2008a). An inverse exposure-rate effect (or protraction enhancement
effect) has also been observed in most analyses (Lubin et al., 1994; NRC, 1998),
although such a modifying effect is not seen at low levels of cumulative WLM
exposure (Lubin et al., 1995; Tomášek et al., 2008a) or was no more evident using
improved individual dosimetric data (Howe, 2006; Vacquier et al., 2009). Models
have been developed to combine the modifying effects of TSE, age and exposurerate. Two models were proposed in the BEIR VI report: the TSE-age-concentration
model and the TSE-age-duration model (NRC, 1998). These models provide risk
coefficients for different windows of cumulative exposure, with additional
modifying effect of age and concentration/duration based on categorical variables.
An alternative approach has been proposed in the joint analysis of the Czech andFrench cohorts, modelling the risk associated with cumulative radon exposure and21

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764

integrating the modifying effects of TSE and AE as continuous variables (Tomášek
et al., 2008a).
(32) For current radiation protection purposes, the most relevant results fromminer studies are those derived for populations with low levels of cumulative
exposure, long duration of follow-up and good data quality. In general, the ERR per
100 WLM estimated from cohorts with low level of exposure (for example, theOntario, Beaverlodge and French cohorts) are higher than those estimated fromcohorts with high levels of cumulated exposures, although the confidence intervals
are broader (Table A3 in Appendix A). Some publications have provided estimates
based on analyses on restricted ranges of exposure (Lubin et al., 1997b). In the
BEIR VI report, such analyses resulted in estimated ERR per 100 WLM of 0.81 and
1.18, below 100 WLM and 50 WLM, respectively (NRC, 1998). In addition,coefficients corresponding to low exposure rates can be obtained from models thattake account of modifying factors. In the BEIR VI report, an ERR per 100 WLM of
3.41 was obtained for low exposure rates < 0.5 WL (TSE-age-concentration model,
for an attained age of 55 - 64 years and at 15-24 years following exposure) (NRC,
1998). Recent analyses from the French and Czech cohorts have provided risk
estimates associated with low levels of exposure and reasonably good quality
exposure assessment (“measured exposures”), with values of ERR per 100 WLMvarying between 2.0 and 3.4 (Tomášek et al., 2008a; Vacquier et al., 2008). A
summary of these risk estimates is presented in Table 3.2, demonstrating significant
associations between cumulative radon exposure and lung cancer mortality at low
levels of cumulative exposure.
Table 3.2 Estimates of the ERR per WLM based on subgroups with low levels of
exposure and low exposure rate
Reference

765
766
767

Model

Exposure

ERR per
CI 95%
100 WLM
0.81
0.30 – 1.42

NRC, 1998

BEIR VI restricted
range< 100 WLM

NRC, 1998

BEIR VI restricted
range< 50 WLM

1.18

0.20 – 2.53

NRC, 1998

BEIR VI TSE-ageconcentration model

rate <0.5 WL

3.41 *-

Howe, 2006

Beaverlodge

Mean 23 WLM

0.96

0.56 – 1.56

UNSCEAR, 2009

Ontario

Mean 31 WLM

0.89

0.5 – 1.5

Vacquier et al.,2008

French cohort,
Mean 17 WLM
employed after 1956

2.0

0.91 – 3.65

Tomášek et al.,
2008a

Joint Czech-Frenchcohort **2.7 *1.7 – 4.3

Mean 47 WLM

CI: Confidence interval - WL: Working level - WLM Working Level Month* for an attained age of 55 - 64 years at 15 – 24 years following exposure** restricted to miners with measured radon exposures

22

DRAFT REPORT FOR CONSULTATION
768

3.3. Lung cancer risks from radon and smoking

769
770
771
772
773
774
775
776
777
778
779
780
781
782
783
784
785
786
787
788
789
790
791
792
793
794
795
796
797

(33) Although smoking is by far the strongest risk factor for lung cancer, moststudies of underground miners could not take account of smoking habits. Several
studies have partial smoking data, including the Chinese Yunnan cohort, theColorado Plateau cohort (United States), the Newfoundland cohort (Canada), theSweden cohort, the New Mexico cohort (United States) and the Radium Hill cohort(South Australia). Case-controls studies among miners have also been conducted toinvestigate the interaction between radon exposure and smoking on lung cancer risk
(Qiao et al., 1989; Lubin et al., 1990; L'Abbe et al., 1991; Thomas, 1994; Yao et al.,
1994; Brüske-Hohlfeld et al., 2006; Leuraud et al., 2007; Amabile et al., 2009).
More information on the lung cancer risk associated with both radon and cigarettesmoking should be available in the future as new datasets from cohort and casecontrol studies are currently under development in Canada (Ontario cohort) and inEurope (Czech, German and French cohorts) (Tirmarche et al., 2009).
(34) Considering currently available data (up to 2009), the results indicate thatthe relationship between lung cancer mortality and radon exposure persists when
account is taken of smoking habits. The analyses conducted for the BEIRVI reportdemonstrated a sub-multiplicative interaction between radon exposure and smoking
status (NRC, 1998). In a recent French nested case-control study, the ERR for lungcancer related to cumulative radon exposure, adjusted for smoking, was 0.85 per 100
WLM (Leuraud et al., 2007), while the value obtained from the total French cohort,when smoking information is ignored, was 0.82 per 100 WLM (Rogel et al., 2002;
Tirmarche et al., 2003). Tirmarche et al. (2003) concluded that presently available
models derived from cohort studies of underground miners that do not take accountof smoking status appear acceptable for the estimation of radon associated lungcancer risks in a population including both smokers and non-smokers. When thesmoking status is known, the estimated ERR generally appears to be larger (even if
not significantly) among non-smokers than among smokers (Lubin et al., 1994;
Tomasek et al., 2002).

23

DRAFT REPORT FOR CONSULTATION
798
799
800

4. ASSESSMENT OF THE DETRIMENT FROM RADON AND RADON
PROGENY EXPOSURE

801

4.1. Risks other than lung cancer

802
803
804
805
806
807
808
809
810
811
812
813
814
815
816
817
818
819
820
821
822
823
824
825
826
827
828
829
830
831
832
833
834
835
836
837
838
839
840
841

(35) Radon and its progeny deliver substantially more dose to the lung than tosystemic organs and the gastrointestinal tract regions. Nevertheless, calculations
indicate that small doses may be received by the red bone marrow and othersystemic organs (Kendall and Smith, 2002; 2005; Khursheed, 2000).
(36) Studies of underground miners generally have not shown any excess ofcancer other than lung cancer to be associated with radon exposure (Darby, 1995;
NRC, 1998; UNSCEAR, 2009). There have been some associations suggested inindividual studies but they have not been replicated in other studies and noconsistent pattern has emerged. For example, recent studies in the Czech Republic
indicated an association with chronic lymphocytic leukaemia incidence (Rericha etal., 2006), but this finding was not confirmed by other studies in the Czech Republic(Tomášek and Malatova, 2006) and in Germany (Möhner et al., 2006). An excess oflarynx cancer suggested in some analyses was also not confirmed in recent studies(Laurier et al., 2004; Möhner et al., 2008). Specific excesses or trends with radon
exposure were noted by recent studies for non-Hodgkin lymphoma, multiple
myeloma, kidney, liver and stomach cancers (Vacquier et al., 2008; Kreuzer et al.,2008, Schubauer-Berigan at al., 2009), but such observations have not been
confirmed by other studies.
(37) Epidemiological studies have been conducted on the possible association
between leukaemia and indoor radon concentrations (Laurier et al., 2001; RaaschouNielsen, 2008). For childhood leukaemia, an association with domestic radon
exposure has been observed in some ecological studies, including the recent findingsof Evrard et al. (2005; 2006). Several large-scale case-control studies which
included alpha-track measurements in the homes of all subjects were unable toconfirm an association between radon exposure and leukaemia risk (Steinbuch et al.
1999; Lubin et al. 1998; UK Childhood Cancer Study Investigators 2002), but arecent study in Denmark suggested a positive significant association between radon
concentrations, estimated on the basis of comprehensive modelling, and acutelymphocytic leukaemia (Raaschou-Nielsen et al., 2008). A recent review concluded
that an association between indoor exposure to radon and childhood leukaemia
might exist, but the current epidemiological evidence is weak and further researchwith better study designs is needed (Raaschou-Nielsen, 2008).
(38) In conclusion, the review of the available epidemiological evidence shows
no consistent evidence for an association between radon concentrations and cancer
other than that of the lung.
(39) It is noted that most available data relate to adult population. While
dosimetric calculations indicate that doses per unit exposure should not differ
appreciably between children and adults (see Appendix, paragraph B 10), more
information is needed to quantify the effects of exposures received duringchildhood.

24

DRAFT REPORT FOR CONSULTATION
842

4.2. Calculation of lung cancer lifetime risk estimates for underground miners

843
844
845
846
847
848
849
850
851
852
853
854
855
856
857
858
859
860
861
862
863
864
865
866
867
868
869
870
871
872
873

(40) Most miner studies have demonstrated the existence of time modifying
factors of the relationship between cumulated radon exposure and lung cancer risk,such as age at exposure or time since exposure. Due to variations in thecharacteristics of the study populations (attained age, duration of follow-up), thedirect comparison of ERR estimates obtained from different cohorts may be
misleading. Account can be taken of such variations in the calculation of the lifetime
risk associated with a specific exposure scenario (Thomas et al., 1992). In outline,
calculation of lifetime risk requires:
1. Risk coefficients derived from an epidemiological study or studies, with orwithout modifying factors such as attained age.
2. A projection model, enabling extrapolation of risk outside the range consideredby the epidemiological study (exposure range, sex, age) and transport to otherpopulations.
3. Background reference rates for all-cause and lung cancer mortality.
4. A scenario of exposure to radon concentrations.
(41) This approach was used in the ICRP Publication 65 to estimate the risk oflung cancer associated with prolonged exposure to radon concentrations based uponstudies of underground miners (ICRP, 1993). Since that, several lifetime risk
estimates have been published (NRC, 1998; EPA, 2003; Tomášek et al., 2008a), butcannot be easily compared due to differences in the nature of the estimates or in theunderlying assumptions. We focus here on estimates of the lifetime excess absoluterisk (LEAR) of lung cancer death from radon and radon progeny, as considered in
ICRP Publication 65, and we exclude those derived for background rates
corresponding to a specific country. We prioritized models derived from pooled
analyses rather than from single studies. The published estimates are summarized inTable 4.1.
Table 4.1 Estimates of the lifetime excess absolute risk (LEAR) of lung cancer
associated with radon and radon progeny concentrations in underground mines (ICRP
Publication 65 scenario of a constant exposure to 2 WLM/y from age 18 to 64y)

ICRP 65(ICRP, 1993)

Projection Background
LEAR
Reference-4
modelreference rates (10 / WLM)
Relative
ICRP 60
2.8
ICRP, 1993
risk

ICRP 65(ICRP, 1993)

Relativerisk

ICRP 103

2.7

Tomášek et al.,2008b

BEIR VI model TSE-age-c(NRC, 1998)

Relativerisk

ICRP 103

5.3

Tomášek et al.,2008b

Czech-French joint model *(Tomášek et al., 2008a)

Relativerisk

ICRP 103

4.4

Tomášek et al.,2008b

Primary risk model

874ICRP 60 reference rates: averaged over males and females and over 5 countries
875ICRP 103 reference rates: averaged over males and females and over asian and euro-american populations
876* model relying on periods of work with the best quality of exposure assessment
877878(42) The scenario of exposure considered in estimating the LEAR shown in
879
Table 4.1 is as proposed in ICRP Publication 65 (ICRP, 1993): constant low level880
exposure to 2 WLM per year during adulthood from 18 years to 64 years, with risk

25

DRAFT REPORT FOR CONSULTATION
881
882
883
884
885
886
887
888
889
890
891
892
893
894
895
896
897
898
899
900
901
902
903
904
905
906
907
908
909
910
911
912
913
914
915
916
917
918
919
920
921
922
923
924
925
926
927
928
929
930
931

estimated up to 90 or 94 years of age. Using the reference background rates of lungcancer from Publication 60 (ICRP, 1991), Publication 65 (ICRP, 1993) adopted a
LEAR for lung cancer (also denoted as the nominal probability coefficient or fatality
probability) of 2.8 10-4 per WLM for radon exposure. Since detriment was entirely
due to lung cancer mortality, the Commission adopted a total detriment coefficient
equal to this fatality coefficient (ICRP, 1993).
(43) Applying the same risk coefficient as in Publication 65 (ICRP, 1993) to thereference background rates found in Publication 103 (ICRP, 2007), Tomášek et al.
(2008b) calculated a LEAR of lung cancer of 2.7 10-4 per WLM. This comparison
shows that the modification of the reference population for background cancer rates
between Publication 60 and Publication 103 has only a small impact on theestimated LEAR.
(44) Using the same scenario of exposure as in Publication 65 (ICRP, 1993) andreference background rates from the Publication 103 (ICRP, 2007), Tomášek et al.
(2008b) also calculated the LEAR using the BEIR VI TSE-age-concentration model(NRC, 1998). This model relies on the combined analysis of data from 11 cohorts ofminers, and takes into account modifying effects of attained age, TSE, and exposure
rate (note that the scenario corresponds only to the lowest category of exposurerate). The LEAR estimate based on this model was 5.3 10-4 per WLM.
(45) Based on the same assumptions (scenario of exposure of Publication 65(ICRP, 1993) and reference background rates from Publication 103 (ICRP, 2007)),
Tomášek et al. (2008b) calculated the LEAR using the model developed from the
combined analysis of the Czech-French cohorts (Tomášek et al., 2008a). This model
used exposure data for the periods of work with the best quality of exposure
assessment. It took account of the modifying effects of age at exposure and TSE. As
the analysis focused on miners with low levels of exposure, no exposure rate effectwas observed in this analysis (Tomášek et al., 2008a). The LEAR estimate based on
the Czech-French model was 4.4 10-4 per WLM (Tomášek et al., 2008a).
(46) Table 4.1 shows a substantial increase in LEAR when using both the BEIR
VI model and the Czech-French model compared to the LEAR estimated using themodel from Publication 65 (ICRP, 1993). Other published lifetime estimates, basedon specific national rates and therefore not directly comparable to the LEAR
estimated in Publication 65 (ICRP, 1993), also support a tendency for an increase in
the estimated lifetime risks compared to earlier values (EPA, 2003). This increase in
LEAR estimates is related in part to consideration of chronic low rate exposures andin part to the increase in the estimated ERR per WLM observed in recent studies.
(47) Additional LEAR calculations were performed by the Task Group in orderto validate the published results, and to provide a sensitivity analysis of the different
underlying hypotheses using different models, scenarios and background rates.
Some calculations were performed independently by different experts to provide aninternal quality check; we especially thank Doug Chambers and Ladislav Tomášek.
Results confirmed the higher LEAR estimated using the BEIR VI model and theCzech-French model. In addition to these models derived from pooled analyses,
other recent models obtained from single studies were also considered (French
CEA-AREVA cohort (Vacquier et al., 2008; Canadian Eldorado cohort (Howe,
2006), German Wismut cohort (Grosche et al., 2006)). It showed that the estimatedLEAR can vary from about 3 to 7 10-4 per WLM according to the model used. These
results illustrate the sensitivity of the estimate to the choice of the model, andreinforced our preference for models derived from pooled analyses. Other
calculations also illustrated the sensitivity of LEAR estimates to background rates.
Using the rates for Euro-American males instead of the reference rates averaged
26

DRAFT REPORT FOR CONSULTATION
932
933
934
935
936
937
938
939
940
941
942
943
944
945
946

over males and females and over Euro-American and Asian populations (ICRP
2007), the estimated LEAR is about 7 10-4 per WLM. This difference is due to thehigher background lung cancer rate among euro-american males. Conversely, using
lower background lung cancer rates (such as females or non smokers) would lead tolower estimated LEAR per WLM.
(48) We conclude that a LEAR of 5 10-4 per WLM (14 10-5 per mJ h m-3),
should now be used as the nominal probability coefficient for radon and radon
progeny induced lung cancer, replacing the ICRP Publication 65 value of 2.8 10-4
per WLM (8 10-5 per mJ h m-3). Current knowledge of radon associated risks fororgans other than the lungs, does not justify the selection of a detriment coefficientdifferent from the fatality coefficient for radon exposure. The estimated lifetime
excess absolute risk of lung cancer death, corresponding to the attributableprobability of fatal lung cancer (or nominal fatality probability coefficient), is
therefore considered to reflect the lifetime detriment associated with radon andradon progeny exposure.

947

4.3. Comparison of results from underground mine and domestic exposures

948
949
950
951
952
953
954
955
956
957
958
959
960
961
962
963
964
965
966
967
968
969
970
971
972
973
974
975
976
977
978
979

(49) The comparison of results obtained from miner studies and from indoor
studies is not straightforward. This is due mainly to the use of different
epidemiological designs (mostly cohort studies for miners and case-control studies
for indoor exposures) as well as different measures of exposure (WLM in mines,
radon gas concentrations in homes). The miner studies have the advantage ofconsidering the evolution over time of the individual radon cumulative exposureand therefore enable the consideration of the modifying effects of age and time since
exposure, but often are unable to consider the effect of cofactors, such as smoking.
The domestic case-control studies have the advantage of providing detailed
information about many potential cofactors, but contemporary measures must be
used to estimate prior radon concentrations during previous decades. They generally
consider only the average radon concentration in a home over a given period and are
not able to analyse potential time modifiers of the exposure - risk relationship.
(50) Estimated primary risk coefficients are presented in Tables 2.1 and 2.2 forindoor studies and Tables 3.1 and 3.2 (and Appendix A) for miner studies.
According to ICRP Publication 65, assuming an occupancy of 7000 h y-1 and an
equilibrium factor (F) of 0.4, a concentration of 1 Bq m-3 radon gas leads to an
exposure of 4.40.10-3 WLM indoor (ICRP, 1993). Most indoor case-control studies
have estimated radon concentrations for periods of 30 or 35 years before diagnosis,
with an exposure - lag time of five years. Therefore, considering a period of 30 years(ie. the last 35 years before diagnosis with a lag time of 5 years) and a time weighted
averaged concentration of 100 Bq m-3, the cumulated exposure of 2.1 107 h Bq m-3
corresponds to a cumulated exposure of approximately 13 WLM assuming F-0.4.
Using these values, an ERR per 100 Bq m-3 of 0.16 for indoor exposures (asobtained in the European pooling study with uncertainty correction; Darby et al.,2006) corresponds to an ERR of 1.2 per 100 WLM, which is similar to the value
obtained in the BEIR VI analysis restricted to low levels of exposure below 50
WLM (NRC, 1998; see Table 3.2). This approach indicates a reasonably good
agreement between the risk coefficients estimated for lung cancer mortality fromindoor studies and miner studies at low levels of exposure. The same reasoning has
been presented by several authors and led to the same conclusion (Zielinski et al.,2006; UNSCEAR, 2009; Tomášek et al., 2008a).
27

DRAFT REPORT FOR CONSULTATION
980
981
982
983
984
985
986
987
988
989
990
991
992
993
994
995
996
997
998
999
1000
1001
1002
1003
1004
1005

(51) The above approach does not consider the modifying effects of age andtime since exposure on the exposure risk relationship demonstrated by miner studies.
Lifetime estimates of lung cancer risk can account for these modifying factors andprovide another method for comparing underground miner study results with thosefrom indoor radon investigations. Nevertheless, due to differences in backgroundrates, duration of life considered and scenario of exposure, considerable caution isneeded in comparing published lifetime estimates obtained from miner studies(ICRP, 1993; NRC, 1998; EPA, 2003; Tomášek et al., 2008a),and from indoor
studies (Darby et al., 2006).
(52) To allow comparison of estimated risks between miner studies and theEuropean indoor study, additional calculations were performed by the Task Group
using parameters chosen to respect as closely as possible the characteristics of theavailable data. A specific scenario was elaborated in order to reflect thecharacteristics of the subjects included in the European indoor study (attained age of
70 years corresponding to the average age at diagnosis, constant exposure to 100 Bq
m-3 over a time window of 5 to 30 years before diagnosis). To reflect the fact thatminer studies provide risk estimates for males, we used the ERR per 100 Bq m-3 of0.25 obtained in the European pooling study for males only (Darby et al., 2006).
Using these parameters, the cumulated absolute risk up to 70 years of age estimatedfor two pooled analyses of miner studies (BEIR VI and French-Czech) and for theEuropean pooled analysis of indoor exposures were 3.5, 2.7 and 2.7 10-4 per WLM,
respectively.
(53) In conclusion, the currently available results show reasonably goodconsistency between lung cancer risk estimates obtained from miner and fromindoor studies.

28

DRAFT REPORT FOR CONSULTATION
1006
1007

5. CONCLUSIONS

1008
1009
1010
1011
1012
1013
1014
1015
1016
1017
1018
1019
1020
1021
1022
1023
1024
1025
1026
1027
1028
1029
1030
1031
1032
1033
1034
1035
1036
1037
1038
1039
1040
1041
1042
1043
1044
1045
1046
1047
1048
1049
1050
1051
1052
1053
1054

(54) This review and analysis of the epidemiology of radon leads to thefollowing conclusions:• There is compelling evidence from cohort studies of underground miners
and from case-control studies of residential radon exposures that radon andits progeny can cause lung cancer. For solid tumours other than lungcancer, and also for leukaemia, there is currently no convincing or
consistent evidence of any excesses associated with radon and radon
progeny exposures.
• The three pooled residential case-control studies (in Europe, North America
and China) gave similar results and showed that the risk of lung cancer
increases at least by 8% for an increase of 100 Bq m-3 in the radon
concentration (Darby et al., 2005; Krewski et al., 2006; Lubin et al., 2004).
• After correcting for random uncertainties in the radon activity concentration
measurements, the European pooled residential case control study gave an
excess relative risk of 16% (5% to 32%) per 100 Bq m-3 increase (Darby etal., 2005). This value may be considered as a reasonable estimate for risk
management purposes at relatively low and prolonged radon exposures inhomes, considering that this risk is linked to an exposure period of at least
25 years.
• There is evidence from the European pooled residential case- control study
that there is a risk of lung cancer even at levels of long-term average radon
concentration below 200 Bq m-3 (Darby et al., 2005).
•• The cumulative risk of lung cancer up to 75 year of age is estimated forlifelong non-smokers as 0.4%, 0.5% and 0.7% for radon activity
concentrations of 0, 100 and 400 Bq m-3, respectively. The lifetime
cumulative risks of lung cancer by age 75 for lifelong smokers are close to10%, 12% and 16% for radon activity concentrations of 0, 100 and 400 Bq
m-3, respectively (Darby et al., 2005; 2006). Cigarette smoking remains themost important cause of lung cancer.
• Appropriate comparisons of lung cancer risk estimates from miner studies
and from indoor studies show good consistency.
• Based upon a review of epidemiological studies of underground miners,
including studies with relatively low levels of exposure, a detrimentadjusted nominal risk coefficient of 5 10-4 per WLM (0.14 per J h m-3) is
adopted for the lung detriment per unit radon exposure. This value of 5 10-4
WLM-1 (0.14 per J h m-3) is derived from recent studies considering
exposure during adulthood and is close to twice the value calculated in
Publication 65 (ICRP, 1993).
(55) Risk estimates obtained from indoor epidemiological studies are
sufficiently robust to enable protection of the public to be now based on residential
concentration levels. ICRP Publication 65 recommended that doses from radon andits progeny should be calculated using a dose conversion convention based on miner
epidemiological studies. No such conversion convention is proposed in the present
report.
(56) For occupational protection purposes, dose estimates are required todemonstrate compliance with limits and constraints. In addition to the review of29

DRAFT REPORT FOR CONSULTATION
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1059
1060
1061
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1063
1064
1065
1066
1067
1068

epidemiology data, the Task Group also reviewed published dose calculations forradon and progeny (see Annex B). The Commission now proposes to treat radon andradon progeny in the same way as other radionuclides within the system ofprotection and publish dose coefficients (dose per unit exposure). Doses from radonand its progeny will be calculated using ICRP biokinetic and dosimetric models,
including the ICRP Publication 66 Human Respiratory Tract Model (HRTM) and
ICRP systemic models. This will apply to thoron (220Rn) and thoron progeny as wellas radon (222Rn) and radon progeny (see Appendix B). Published values of effective
dose from radon progeny inhalation derived using the HRTM range from about 10
to 20 mSv WLM-1 (3 to 6 mSv per mJ h m-3) depending on the scenario of exposure.
Reference ICRP dose coefficients per unit exposure to radon and its progeny will be
published for different reference conditions of exposure, with specified aerosol
characteristics and equilibrium factors. Until these dose coefficients are published,
the previously recommended values (ICRP 1993) should continue to be used.

1069
1070

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REFERENCES

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1283

APPENDIX A.

1284

Results from epidemiological studies of underground miners

1285

Table A1 Characteristics of the cohorts used in ICRP Publication 65 (ICRP, 1993)

1286
1287

CountryType ofmine

Follow-up
periodNbminers

Cumul
expo
WLM

Personyears *ERR per
100 WLM

95% CI

Colorado *USA

Uranium

1951-82

2 975

510

66 2370.60

0.30-1.42

Ontario

CanadaUranium

1955-81

11 07637217 8101.42

0.60-3.33

New Mexico

USA

Uranium

1957-85

3 469

111

66 5001.81

0.71-5.46

Beaverlodge

CanadaUranium

1950-806 895

44114 170

1.31

0.60-3.01

West Bohemia

Czech Rep. Uranium

1953-85

4 042

227

97 913

1.70

1.21-2.41

Cea-Cogema

FranceUranium

1946-851 785

70

44 0050.60

0.00-1.63

Malmberget

SwedenIron

1951-76

1 292

98

27 3971.42

0.30-9.57

31 486
CI : confidence interval

120

635 022
1.34* < 2000 WLM

0.82-2.13

Name-place

Total
1288
ERR : excess relative risk
1289
1290

35

DRAFT REPORT FOR CONSULTATION
1291
1292
1293

Table A2 Characteristics of the cohorts considered in the BEIR VI report (NRC, 1998)
CountryType ofmine

Follow-up
Nbperiodminers *

Cumul
expo
WLM

Personyears *ERR per
100 WLM

YunnanChina

Tin

1976-87

13 649286.0

134 842

0.17

W-Bohemia

Czech Rep. Uranium

1952-90

4 320

196.8

102 650

0.67

Colorado

USA

Uranium

1950-90

3 347

578.6

79 5560.44

Ontario

CanadaUranium

1955-86

21 34631.0

300 608

0.82

Newfoundland

CanadaFluorspar

1950-84

1 751

388.4

33 795

0.82

Malmberget

SwedenIron

1951-91

1 294

80.6

32 452

1.04

New Mexico

USA

Uranium

1943-85

3 457

110.9

46 8001.58

Beaverlodge

CanadaUranium

1950-80

6 895

21.2

67 0802.33

Port Radium

CanadaUranium

1950-80

1 420

243.0

31 454

0.24

Radium Hill

Australia

Uranium

1948-87

1 457

7.6

24 138

2.75

Cea-Cogema

FranceUranium

1948-86

1 769

59.4

39 1720.51

Name-place

1294
1295

Total
ERR : excess relative risk

60 606164.4
se: multiplicative standard error

36

888 906
0.59* among exposed

se

1.32

DRAFT REPORT FOR CONSULTATION
Table A3 Characteristics of the cohorts considered by UNSCEAR (2009)

1296
1297

Type ofmine

Follow-up
periodNbminersCumulative
exposure
WLM

Uranium

1950-90

3347

Newfoundland Canada

Fluorspar

1951-01

YunnanChina

Tin

WismutGermany

Malmberget

Sweden

W-Bohemia

Person ERR per-years 100 WLM

CI 95%

807

75 0320.42

0.3 – 0.7

1742

378

70 8940.47

0.28 - 0.65

1976-87

13 649277

0.16

0.1 – 0.2

Uranium

1946-98

59 001242

0.21

0.18 – 0.24

Iron

1951-90

1415

81

0.95

0.1 – 4.1

Czech Rep. Uranium

1952-99

9979

70

1.60

1.2 – 2.2

Cea-Cogema

FranceUranium

1946-94

5098

37

0.80

0.3 – 1.4

Ontario

CanadaUranium

1955-86

21 34631

0.89

0.5 – 1.5

Beaverlodge

CanadaUranium

1950-99

10 05023

0.96

0.56 – 1.56

0.59

0.35 – 1.0

Name-place
Colorado

Country
USA

Total
1298
1299

ERR : excess relative risk

125 627

135
357
1 801
626
32 452
261
428
133
521
319
701
285
964
3 115
975

CI : confidence interval

1300

References for Appendix A

1301
1302
1303
1304
1305
1306
1307
1308
1309

ICRP, 1993. Protection against radon-222 at home and at work. ICRP Publication 65. Ann.
ICRP 23(2).
NRC, 1998. Committee on Health Risks of Exposure to Radon. Board on Radiation Effects
Research. Health effects of exposure to radon. BEIR VI report. National Academy Press,
Washington, D.C., National Research Council.
UNSCEAR, 2009. UNSCEAR 2006, Annexe E “Sources-to-effects assessment for radon inhomes and workplaces. United Nations Scientific Committee on the Effects of Atomic
Radiation. United Nations, New York.

37

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1310

APPENDIX B.

DOSIMETRY

1311

B.1. Radon

1312
1313
1314
1315
1316
1317
1318
1319
1320
1321
1322
1323
1324
1325
1326
1327
1328
1329
1330
1331
1332
1333
1334
1335
1336
1337
1338
1339
1340
1341
1342
1343
1344
1345
1346
1347
1348
1349
1350
1351
1352
1353
1354
1355

(B 1) The equivalent dose to the lung following the inhalation of radon and its
short-lived progeny can be calculated using the ICRP Human Respiratory Tract
Model (HRTM) (ICRP, 1994) and other models of the human respiratory tract.
Nearly the entire lung dose arises from the inhalation of the radon progeny and notfrom the gas itself as almost all of the gas that is inhaled is subsequently exhaled.
However, a large proportion of the inhaled radon progeny deposits in the respiratory
airways of the lung. Because of their short half-lives (less than half an hour), doseis delivered to the lung tissues before clearance can take place, either by absorption
into blood or by particle transport to the alimentary tract. Two of the short-lived
radon progeny (218Po, 214Po) decay by alpha particle emission and it is the energy
from these alpha particles that accounts for the relatively high dose to the lung. In
comparison, doses to systemic organs and gastrointestinal tract regions are low andcan be ignored in the calculation of effective dose. The equivalent dose to theextrathoracic region is not small but its contribution to the effective dose is quite
small.
(B 2) The radon progeny aerosol in the atmosphere is created in two steps.
After decay of the radon gas, the freshly formed radionuclides (218Po, 214Pb, 214Bi)
react rapidly (< 1 s) with trace gases and vapours and grow by cluster formation toform particles around 1 nm in size. These are referred to as unattached particles.
The unattached particles may also attach to existing aerosol particles in theatmosphere within 1 – 100 s forming the so-called attached particles. The attachedparticles can have a trimodal activity size distribution which can be described by asum of three lognormal distributions (Porstendörfer, 2001). These comprise thenucleation mode with an activity median aerodynamic diameter (AMAD) between
10 nm and 100 nm, the accumulation mode with AMAD values 100 – 400 nm and acoarse mode with an AMAD > 1 μm. Generally, the greatest activity fraction is in
the accumulation mode which has a geometric standard deviation of about 2.
(B 3) A dosimetric model for the respiratory tract needs to describe themorphometry, the deposition of the inhaled material, clearance from the respiratory
tract and the location of target tissues and cells at risk. For radon progeny, it is thedose to the target cells in the bronchial and bronchiolar regions of the lung that areof importance. In comparison, the dose to the alveolar region is significantly lower(UNSCEAR 1982, Marsh and Birchall, 2000).
(B 4) ICRP (1987) used values of dose per unit radon exposure based on an
NEA (1983) review of available dosimetric models (Jacobi and Eisfed, 1980, 1982,
James et al. 1982, Harley and Pasternack, 1982, Hofmann et al. 1980). UNSCEAR(1982; 1988; 1993) used similar estimates of dose from radon inhalation and the2000 report retained a value of effective dose of 5.7 mSv WLM-1 (1.6 mSv permJ h m-3, i.e. 9 nSv per Bq h m-3 of equilibrium equivalent concentration (ECC) of
radon) for indoor and outdoor exposures (Table B.1). In the 2000 report, UNSCEAR
recognised that more recent calculations with new dosimetric models resulted inhigher values of this dose conversion factor. However, because of the lower values
calculated using the dose conversion convention (ICRP, 1993), it was concluded that38

DRAFT REPORT FOR CONSULTATION
1356
1357
1358
1359
1360
1361
1362
1363
1364

the previous value of 9 nSv per Bq h m-3 (ECC) should continue to be used in dose
evaluations (UNSCEAR, 2000, 2009).

Table B.1 Published values of effective dose to an adult male from the inhalation ofradon and progeny calculated using dosimetric models
Publication

Model TypeICRP 50, 1987

NEA, 1983

UNSCEAR,
2000
Harley et al.,
1996
Porstendörfer,
2001

NEA, 1983

Winkler-Heiland Hofmann,
2002
Winkler-Heil etal., 2007

Deterministic
airway generation
model
Deterministic
airway generation
model
Stochastic airway
generation model
HRTMd
HRTMd

Zock et al., 1996

Exposure
scenario
Indoors
Outdoors
Indoors andoutdoors
Indoors and
mines
Homeb
Work place
OutdoorHome

Effective
Effective dose
dose
-3
-1 mSv per mJ h m
mSv WLM
6.4
1.8
8.9
2.5
5.7
1.6
9.6a

2.7

8
11.5
10.6
7.6

2.3
3.2
3.0
2.1

Mine

8.3

2.3

Mine

8.9

2.5

Mine
Home

11.8
15

3.3
4.2

Marsh andBirchall, 2000
James et al.,
HRTMd
Minec
20.9
5.9
b
2004
Home
21.1
6.0
Marsh et al.,
HRTMd
Mine
12.5
3.5
b
2005
Home
12.9
3.6
a
1365
A value of an absorbed dose of 6 mGy WLM-1 (1.7 mGy per mJ h m-3) was
1366
calculated for the bronchial region. The effective dose per unit exposure was
1367
then calculated with a radiation weighting factor for alpha particles of 20 and a1368
tissue weighting factor of 0.08 (= 2/3 ×0.12) for lung (ICRP, 1993).
b
1369
Home without cigarette smoke.
c1370
No hygroscopic growth was assumed.
d1371
HRTM: Human Respiratory Tract Model (ICRP, 1994).
1372
1373
1374
1375
1376
1377
1378
1379

(B 5) Table B.1 also shows values of effective dose per unit radon progeny
exposure (mSv per WLM or mSv per mJ h m-3) calculated using the ICRP
Publication 66 Human Respiratory Tract Model (HRTM) (ICRP, 1994) and othermodels, including deterministic airway generation models (Winkler-Heil and
Hofmann, 2002, Porstendörfer, 2001, Harley et al. 1996) and a stochastic airway
generation model (Winkler-Heil et al. 2007). Results of selected recent calculations
39

DRAFT REPORT FOR CONSULTATION
1380
1381
1382
1383
1384
1385
1386
1387
1388
1389
1390
1391
1392
1393
1394
1395
1396
1397
1398
1399
1400
1401
1402
1403
1404
1405
1406
1407
1408
1409
1410
1411
1412
1413
1414
1415
1416
1417
1418
1419
1420
1421
1422
1423
1424
1425
1426
1427
1428
1429
1430

are given in Table B.1; more comprehensive tabulations of values publishedbetween 1956 and 1998 are given by UNSCEAR (2000).
(B 6) The main sources of variability and uncertainty in the calculation of theequivalent dose to the lung per unit radon progeny exposure include:• the activity size distribution of the radon progeny aerosol,• breathing rates,• the model used to predict aerosol deposition in the respiratory tract,• the absorption of the radon progeny from lung to blood,• the identification of target cells and their location within bronchial andbronchiolar epithelium,• the relative sensitivity of different cell types to radiation,• the regional differences in the radiation sensitivity of the lung.
Marsh and Birchall (2000) performed a sensitivity analysis to identify those HRTM
parameters that significantly affect the equivalent dose to lung (Hlung) per unit
exposure to radon progeny under conditions found in houses. Other sensitivity
analyses have been reported (NCRP, 1984; NRC, 1991; Zock et al., 1996; Tokonami
et al., 2003) and UNSCEAR (1988) noted that equivalent dose may vary by a factor
of about 3 according to the target cells considered.
(B 7) Winkler et al. (2007) compared the results of the effective dose for radon
progeny inhalation obtained using the HRTM, a deterministic airway generation
model and a stochastic airway generation model, with the same input parametervalues. Similar results were obtained ranging from 8.3 to 11.8 mSv WLM-1 (2.3 to
3.3 mSv per mJ h m-3) (Table B.1). The authors noted that one of the important
issues affecting the comparison is the averaging procedure for the doses calculated
in airway generation models.
(B 8) Porstendörfer (2001) calculated doses from radon progeny exposure fordifferent exposure scenarios using an airway generation model developed by Zock etal. (1996). The effective dose calculated for ‘normal’ aerosol conditions in homes,
workplaces and outdoors ranged from 8.0 to 11.5 mSv WLM-1 (2.3 to 3.3 mSv permJ h m-3) (Table B.1). However, in places with one dominating aerosol source
producing a high number particle concentration (e.g. cigarette smoking or
combustion aerosols by diesel engines) the effective dose was calculated to belower, ranging from 4.2 to 7.1 mSv WLM-1 (1.2 to 2.0 mSv per mJ h m-3). The
activity size distributions and unattached fractions assumed for these calculations
were based upon their measurements in indoor and outdoor air, and in the air atdifferent workplaces in Germany.
(B 9) James et al. (2004) calculated effective doses from radon progeny formines and homes using the HRTM. The activity size distributions given in the
BEIR VI report (NRC, 1998) were assumed. The authors calculated a range ofvalues for mines (18 – 21 mSv WLM-1; 5.1 – 5.9 mSv per mJ h m-3) and homes(16 – 21 mSv WLM-1; 4.5 – 5.9 mSv per mJ h m-3) depending upon whether or not
the attached particles double in size in the respiratory tract due to hygroscopic
growth and depending upon the presence or absence of cigarette smoke in homes.
These estimates are higher compared with other estimates (Table B.1), mainly
because the activity size distribution assumed differed from those used by otherinvestigators. Marsh et al. (2005), also using the HRTM and activity size
distributions for mines and homes based upon measurements carried out in Europe,
calculated values of about 13 mSv WLM-1 (3.7 mSv per mJ h m-3) for mines andhomes (Table B.1).
(B 10) Calculations performed with the HRTM showed that the equivalent doseto lung per unit exposure is relatively insensitive to age (BEIR VI, 1999, Marsh and40

DRAFT REPORT FOR CONSULTATION
1431
1432
1433
1434
1435
1436
1437
1438
1439
1440
1441
1442
1443
1444
1445
1446
1447
1448
1449
1450
1451
1452
1453
1454

Birchall, 2000; Marsh et al., 2005, Kendall and Smith, 2005). For example the lungdose for an adult compared with that of children (> 1y) differs only by about 10%.
The reason for this is that there are competing effects that tend to cancel out.
Children have lower breathing rates which decreases the intakes and lung doses,
while this is partly compensated by the smaller mass of target tissue which increases
the doses. Also children have smaller airways which increase deposition bydiffusion, but this is also compensated in part by smaller residence times that
decrease deposition by diffusion.
(B 11) The values of effective dose from radon progeny inhalation derived fromthe HRTM range from about 10 to 20 mSv WLM-1 (3 to 6 mSv per mJ h m-3)
depending on the scenario of exposure. For typical aerosol conditions in home andmines the effective dose is about 13 mSv WLM-1 (3.7 mSv per mJ h m-3) (Marsh etal., 2005). However, assuming the same aerosol conditions as for a home but with abreathing rate for a standard worker (1.2 m-3 h-1) the effective dose increases from
13 mSv WLM-1 (3.7 mSv per mJ h m-3) to about 20 mSv WLM-1 (6 mSv per mJ h
m-3).
(B 12) The Commission has concluded that doses from radon progeny should be
calculated using ICRP biokinetic and dosimetric models, including the HRTM andthe ICRP systemic models. In other words, radon progeny should be treated in thesame way as any other radionuclide within the system of protection. One of theadvantages of this approach is that doses to organs other than lung can also be
calculated. ICRP will provide dose coefficients per unit exposure to radon progeny
for different reference conditions of domestic and occupational exposure (i.e. of
equilibrium factor and aerosol characteristics).

1455

B.2. Thoron

1456
1457
1458
1459
1460
1461
1462
1463
1464
1465
1466
1467
1468
1469
1470
1471
1472
1473
1474
1475
1476
1477
1478

(B 13) Thoron (220Rn) gas is a decay product of radium-224 and is part of thethorium-232 decay series. Thoron (220Rn) has a short half-live (56 s) and decays
into a series of solid short-lived radioisotopes, including lead-212 which has a
half-life of 10.6 h. Because of the short half-life of thoron, it is less able than radon(222Rn) to escape from the point where it is formed. As a consequence, building
materials are the most usual source of indoor thoron exposure.
(B 14) As for radon, doses from the inhalation of thoron and progeny are
dominated by alpha particle emissions from decay of the progeny (Jacobi andEisfed, 1980, 1982).
Because of its very short half-life, the gas activity
concentration of thoron can vary substantially across a room and so it is not possible
to use thoron gas concentration in dose evaluation. Therefore, for control purposes,
the potential alpha energy concentration of the thoron progeny should be determined
for the estimation of thoron exposure. However, it is usually sufficient to control
the intake of 212Pb for protection purposes because the potential alpha energy (PAE)per unit activity inhaled is about 10 times higher for 212Pb than for other thoron
progeny (ICRP, 1987).
(B 15) UNSCEAR (2000) and the BEIR VI committee (NAS, 1999) presented
data for the ratio of potential alpha energy concentration (PAEC) arising fromthoron (220Rn) progeny to that from radon (222Rn) progeny. The values ranged from
0.1 to 5. The highest values were for wood-frame and mud houses found in Japanand for some houses in Italy that used building materials of volcanic origin.
UNSCEAR also noted that in the UK, a value as high as 30 was observed for ahouse with a high ventilation rate and an unusually low radon concentration
41

DRAFT REPORT FOR CONSULTATION
1479
1480
1481
1482
1483
1484
1485
1486
1487
1488
1489
1490
1491
1492
1493
1494
1495
1496
1497
1498
1499
1500
1501
1502
1503
1504
1505

1506
1507
1508
1509
1510
1511
1512
1513
1514
1515

(UNSCEAR, 2000, Cliff et al. 1992). The BEIR VI committee concluded that fordwellings with high radon (222Rn) concentrations, it appears that the thoron (220Rn)progeny will not be an important additional source of exposure and dose (NRC,
1999).
(B 16) A summary of dose coefficients for thoron progeny, calculated using
dosimetric models, is given in Table B.2. Values range from 1.5 – 5.7 mSv WLM-1
i.e. 0.42 - 1.6 mSv per mJ h m-3 or 10 – 122 nSv per Bq h m-3 (EEC).
(B 17) The dose coefficient given in ICRP Publication 50 (ICRP, 1987) is basedon the work of an Expert Group of OEC/NEA (NEA, 1983), which reviewed themodels of Jacobi and Eisfed (1980; 1982) and of James et al. (1980; 1982). Only
doses to the bronchial epithelium and pulmonary tissue were considered.
(B 18) In its 1982 report, UNSCEAR not only considered the doses to the lungbased upon the work of Jacobi and Eisfed (1980) but also considered doses to othertissues by applying the dosimetric models given in ICRP Publication 30 (ICRP,
1979). Values of 1.9 mSv WLM-1 (0.54 mSv per mJ h m-3) and 2.5 mSv WLM-1(0.71 mSv per mJ h m-3) were recommended for indoor and outdoor exposures,
respectively. The effective dose coefficients for thoron progeny given in the 1988
UNSCEAR report were based upon the calculations of Jacobi and Eisfed (1982) andcorresponded to an effective dose per unit PAE of 0.7 mSv mJ-1. These values wereretained in the 1993 report (UNSCEAR, 1993) and are given in Table B.2.
UNSCEAR (2000, 2009) has since adopted a value 40 nSv per h Bq m-3 (ECC) (i.e.
1.9 mSv per WLM or 0.54 mSv per mJ h m-3) for indoors and outdoor exposures,
which is similar to the value given in ICRP Publication 50 (ICRP, 1987).
Table B.2 A summary of the calculated dose conversion factors(a) for thoron progeny using
direct dosimetry.
Publication

Model Type

Exposure
scenario

Effectivedose(b)mSv WLM-1

Effective dose,-3
mSv per mJ h m

ICRP 50, 1987

NEA (1983)

1.8

0.51

UNSCEAR,
1993
Marsh andBirchall, 1999
Porstendörfer,
2001
Ishikawa et al.,2007
Kendall andPhipps, 2007

Jacobi and Eisfed, 1982

Indoors andoutdoors
Indoors
Outdoors
Dwellings

1.5
0.47
3.8

0.42
0.13
1.1

HRTM, (ICRP, 1994)

Indoors
Outdoors
Indoors

2.4
2.0
5.4

0.68
0.56
1.5

HRTM, (ICRP, 1994)

Indoors

5.7

1.6

HRTM, (ICRP, 1994)
Zock et al. (1996)(a) Calculated for an adult male(b) 1 WLM = 4.68 104 Bq h m-3 of EEC of 220Rn.

(B 19) The values of the dose coefficients obtained using the HRTM (Marsh andBirchall, 1999; Ishikawa et al., 2007, Kendall and Phipps, 2007) are higher than thevalues recommended by ICRP (1987) and UNSCEAR (1993). Kendall and Phipps(2007) calculated the effective dose conversion factor for thoron progeny with the
HRTM and the most recent biokinetic models for lead (ICRP, 1993) and bismuth(ICRP 1979). The authors showed that typically the dose to the lung contributed
42

DRAFT REPORT FOR CONSULTATION
1516
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1519
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1521

more than 97% of the effective dose and that the intake from 212Pb alone contributes
to about 85% of the total dose. Calculations for different age groups (> 1 y) showedthat the dose per unit exposure differed by 10% or less (Kendall and Phipps, 2007).
(B 20) Following the decision to treat radon isotopes in the same way as otherradionuclides for protection purposes, biokinetic and dosimetric models will be used
to provide dose coefficients for radon-220 as well as radon-222.

1522

References for Appendix B

1523
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1534
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1537
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1542
1543
1544
1545
1546
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1553
1554
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1565
1566

Cliff, K.D., Green, B.M.R., Mawle, A., et al., 1992. Thoron daughter concentrations in UK
homes. Radiat. Prot. Dosim. 45(1/4), 361-366.
ICRP, 1979. Limits for Intakes of Radionuclides by Workers, Part 1. ICRP Publication 30.
Ann. ICRP 2(3-4).
ICRP, 1987. Lung cancer risk from indoor exposures to radon daughters. ICRP Publication
50. Ann. ICRP 17(1).
ICRP, 1993. Protection against radon-222 at home and at work. ICRP Publication 65. Ann.
ICRP 23(2).
ICRP, 1994. International Commission on Radiological Protection. Human respiratory tract
model for radiological protection. ICRP Publication 66. Ann. ICRP 24(1-3).
Ishikawa, T., Tokonami, S., and Nemeth, C., 2007. Calculation of dose conversion factors
for thoron decay products. J. Radiol. Prot. 27 447-456.
Jacobi, W. and Eisfeld, K., 1980. Dose to tissues and effective dose equivalent byinhalation of radon-222, radon-220 and their short-lived daughters. GSF-S-626
Neuherberg, GSF.
Jacobi, W. and Eisfeld, K., 1982. Internal dosimetry of inhaled radon-222, radon-220 andtheir short-lived daughters. Proc. 2nd Special Symp. On the Natural Radiation
Ennvironment (Bhaba Atomic Research Centre, Bombay, India, Jan. 1981) ed K G
Vohra, U C Mishra, K C Pillai and S Sadavisan (New Delhi: Wilet Eastern) pp 131-43.
James, A.C., Greenhalgh, J.R. and Birchall, A., 1980. A dosimetric model for tissues of thehuman respiratory tract at risk from inhaled radon and thoron daughters. Radiation
Protection  A Systematic Approach to Safety, Proc. 5th Congr. IRPA (Jerusalem,1980) vol 2 (Oxford: Pergamon) pp 1045-8.
James, A.C., Jacobi W. and Steinhäusler, F., 1982. Respiratory tract dosimetry of radon andthoron daughters.
The state-of-the-art and implications for epidemiology andradiobiology. p. 42-54 in: Radiation Hazards in Mining: Control, Measurements andMedical Aspects. (M. Gomez,ed.), Soc. Mining Engineers, New York.
James, A.C., Birchall, A. and Akabani, G., 2004. Comparative dosimetry of BEIR VI
revisited. Radiat. Prot. Dosim. 108(1), 3-26.
Kendall, G.M. and Phipps, A.W., 2007. Effective and organ doses from thoron decay
products at different ages. J. Radiol. Prot. 27, 427-435.
Marsh, J.W. and Birchall, A., 1999. The thoron issue: monitoring activities, measuring
techniques and dose conversion factors. Radiat. Prot. Dosim. 81(4), 311-2 (Letter to the
Editor).
Marsh, J.W., Birchall, A. and Davis, K., 2005. Comparative dosimetry in homes and mines:
estimation of K-factors. Natural Radiation Environment VII. Seventh International
Symposium on the Natural Radiation Environment (NRE-VII). Radioactivity in theEnvirnoment, Vol. 7, Elsevier Ltd. ISSN 1569-4860.
NEA, 1983. Dosimetry aspects of exposure to radon and thoron daughters products. Nuclear
Energy Agency Report NEA/OECD, Paris.
NRC, 1988. Health risks of radon and other internally deposited alpha emitters. BEIR IV
report. National Academy Press. ISBN 0-309-03789-1, National Research Council.
NRC, 1991. Comparative dosimetry of radon in mines and homes. National Academy
Press, Washington, DC, National Research Council. ISBN 0-309-04484-7.

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1567
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1585
1586
1587
1588

NRC, 1998. Committee on Health Risks of Exposure to Radon. Board on Radiation Effects
Research. Health effects of exposure to radon. BEIR VI report. National Academy Press,
Washington, D.C., National Research Council.
Porstendörfer, J., 2001. Physical parameters and dose factors of the radon and thoron decay
products. Radiat. Prot. Dosim. 94(4), 365-373.
UNSCEAR, 1982. United Nations Scientific Committee on the Effects of Atomic Radiation.
Sources and effects of ionizing radiation. 1982 Report to the General Assembly with
Annexes, United Nations, New York.
UNSCEAR, 1993. United Nations Scientific Committee on the Effects of Atomic Radiation.
Sources and effects of ionizing radiation. 1993 Report to the general Assembly with
scientific annexes, United Nations, New York.
UNSCEAR, 2000. Sources and effects of ionizing radiation. United Nations ScientificCommittee on the Effects of Atomic Radiation UNSCEAR 2000 report to the general
assembly with scientific annexes, United Nations, New York.
UNSCEAR, 2009. UNSCEAR 2006, Annexe E “Sources-to-effects assessment for radon inhomes and workplaces. United Nations Scientific Committee on the Effects of Atomic
Radiation. United Nations, New York.
Zock, C., Porstendörfer, J. and Reineking, A., 1996. The influence of the biological andaerosol parameters of inhaled short-lived radon decay products on human lung dose.
Radiat. Prot. Dosim., 63(3), 197-206.

44